Fruits of orange-fleshed and green-fleshed muskmelon (Cucumis melo L.) were harvested at different times throughout development to evaluate changes in metabolism which lead to sucrose accumulation, and to determine the basis of differences in fruit sucrose accumulation among genotypes. Concentrations of sucrose, raffinose saccharides, hexoses and starch, as well as activities of the sucrose metabolizing enzymes sucrose phosphate synthase (SPS) (EC 2.4.1.14), sucrose synthase (EC 2.4.1.13), and acid and neutral invertases (EC 3.2.1.26) were measured. Sucrose synthase and neutral invertase activities were relatively low (1.7 ± 0.3 micromole per hour per gram fresh weight and 2.2 ± 0.2, respectively) and changed little throughout fruit development. Acid invertase activity decreased during fruit development, (from as high as 40 micromoles per hour per gram fresh weight) in unripe fruit, to undetectable activity in mature, ripened fruits, while SPS activity in the fruit increased (from 7 micromoles per hour per gram fresh weight) to as high as 32 micromoles per hour per gram fresh weight. Genotypes which accumulated different amounts of sucrose had similar acid invertase activity but differed in SPS activity. Our results indicate that both acid invertase and SPS are determinants of sucrose accumulation in melon fruit. However, the decline in acid invertase appears to be a normal function of fruit maturation, and is not the primary factor which determines sucrose accumulation. Rather, the capacity for sucrose synthesis, reflected in the activity of SPS, appears to determine sucrose accumulation, which is an important component of fruit quality.Midway through development, muskmelon (Cucumis melo L.) fruits undergo a metabolic transition marked by both physical and compositional changes such as netting of the exocarp, mesocarp softening, and the onset of sucrose accumulation (1,7,10,12

Continuous exposure of tomato`Trust' to high temperatures (day/night temperatures of 32/26°C) markedly reduced the number of pollen grains per¯ower and decreased viability. The effect of heat stress on pollen viability was associated with alterations in carbohydrate metabolism in various parts of the anther during its development. Under control, favourable temperature conditions (28/22°C), starch accumulated in the pollen grains, where it reached a maximum value 3 d before anthesis; it then diminished towards anthesis. During anther development, the concentration of total soluble sugars gradually increased in the anther walls and in the pollen grains (but not in the locular¯uid), reaching a maximum at anthesis. Continuous exposure of the plants to high temperatures (32/26°C) prevented the transient increase in starch concentration and led to decreases in the concentrations of soluble sugars in the anther walls and the pollen grains. In the locular¯uid, however, a higher soluble sugar concentration was detected under the high-temperature regime throughout anther development. These results suggest that a major effect of heat stress on pollen development is a decrease in starch concentration 3 d before anthesis, which results in a decreased sugar concentration in the mature pollen grains. These events possibly contribute to the decreased pollen viability in tomato.

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Reactive oxygen species (ROS) are both signal molecules and direct participants in plant defense against pathogens. Many fungi synthesize mannitol, a potent quencher of ROS, and there is growing evidence that at least some phytopathogenic fungi use mannitol to suppress ROSmediated plant defenses. Here we show induction of mannitol production and secretion in the phytopathogenic fungus Alternaria alternata in the presence of host-plant extracts. Conversely, we show that the catabolic enzyme mannitol dehydrogenase is induced in a non-mannitol-producing plant in response to both fungal infection and specific inducers of plant defense responses. This provides a mechanism whereby the plant can counteract fungal suppression of ROS-mediated defenses by catabolizing mannitol of fungal origin.Compelling evidence has arisen over the last decade demonstrating that reactive oxygen species (ROS) play a central role in pathogen defense in both animals and plants. In animals, ROS production by phagocytic leukocytes (macrophages͞ neutrophils) is a well characterized antimicrobial defense mechanism (1). Plants produce an analogous, localized oxidative burst (2), wherein massive amounts of antimicrobial ROS [e.g., superoxide, ⅐O 2 Ϫ ; and hydrogen peroxide (H 2 O 2 )] are generated by a pathogen-induced NADPH oxidase localized on the plant plasma membrane (3). In addition to its direct antimicrobial activity, H 2 O 2 also triggers the hypersensitive response, in which plant programmed, localized cell death at the site of infection limits pathogen spread (4). H 2 O 2 also plays a central role in signaling a unique phenomenon known as systemic acquired resistance, in which localized infection of a plant confers enhanced systemic resistance to subsequent attack by the same or unrelated pathogens (5, 6). Systemic acquired resistance is correlated with the systemic induction of a large number of defense-related proteins collectively labeled pathogenesis-related (PR) proteins. In addition to H 2 O 2 , the endogenous signal molecule salicylic acid (SA) is implicated in PR protein induction and has been used extensively as an exogenous stimulator of the systemic acquired resistance response (7,8).A successful pathogen must be able to overcome or suppress this complex array of ROS-mediated host defenses. In fact, microbial suppression of ROS-mediated defenses by secretion of ROS-scavenging enzymes such as superoxide dismutase and catalase, which convert ROS into less reactive species, has been extensively documented in both plant and animal pathogens (9-12). Evidence also is emerging that pathogens suppress ROS-mediated defenses by nonenzymatic quenching of ROS. Mannitol has long been recognized as a potent ROS quencher in vitro (13) and has widely been used as a laboratory reagent to scavenge hydroxyl radicals (HO⅐) generated by the phagocyte respiratory burst or by cell-free oxidant systems (14). In vivo, increased mannitol production protects Saccharomyces cerevisiae from oxidative injury (15). Furthermore, it was recently show...